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• W1584614998 abstract "Angiogenesis is the process by which blood microvessels are formed from existingones. Angiogenesis is required for development. It is also important for reducingmyocardial hypoxia due to coronary and ischemic heart disease; in myocardialinfarction or chronic ischemic heart disease angiogenesis responds to tissue hypoxiaby new vessel formation (angiogenesis), which diminishes myocardial ischemia.However, physiological angiogenesis is usually insufficient to re-establish anadequate blood supply to the myocardium, which decreases its proper functioning.Therapeutic angiogenesis in the heart aims at increasing new vessel formation inischemic myocardium and thus improving myocardial function by increasing bloodflow (oxygen and nutrient supply). This may contribute to preventing heart failureand sudden cardiac death. Unfortunately no assay is available to investigate questionsaround angiogenesis in an easy format and in a way that does not use big numbers ofanimals.Angiogenesis and hypertension are intrinsically linked; angiogenesis is impaired inhypertension, and microvascular rarefaction is a mainstay of hypertension-inducedtarget organ damage. Many metabolic pathways, for example the Renin-Angiotensin-Aldosterone-System (RAAS) or Nitric Oxide (NO), are involved in the developmentof hypertension, hypertension-induced target organ damage and also angiogenesis.Contrariwise, treatment of hypertension by drugs such as ACE-inhibitors not onlyreduces blood pressure and hypertension-induced target organ damage but alsoimproves angiogenesis and thus tissue oxygenation. Specifically, accumulation ofBradykinin in response to ACE inhibition may result in angiogenesis. A study in ourlaboratory lead us to conclude that impaired angiogenesis in hypertension may resultfrom impaired NO biosynthesis and not from elevated blood pressure itself. Inaddition, activation or RAAS or other factors may affect angiogenesis inhypertension.The general aim of this thesis was to first contribute at developing a new angiogenesisassay of the heart in vitro and to then use it to investigate the role of Angiotensin IIand Nitric Oxide on angiogenesis in the heart in vitro, independent of blood pressure.We also aimed at understanding mechanisms involved in these responses.In order to further study questions of angiogenesis and hypertension in a relevanttarget organ, we developed and validated a new in vitro assay for investigatingangiogenesis of the heart. At the time most experiments were being performed in vivosince no appropriate in vitro model was available. In vivo experiments require a largenumber of animals, are difficult to perform and are often associated with pain to theanimals and their death. Our new in vitro model solved or reduced some of theseproblems. We found that both hypoxia and serum (5%) are required for angiogenesisto occur in the adult mouse heart in vitro. We analyzed the morphology of thedifferent sprouts and found they were always composed by endothelial cells, and thatsmooth muscle cells or pericytes align along the sprouts. We conclude thatangiogenesis of the heart in vitro can be investigated with a simple assay that allows alarge series of experiments to be carried out in a relatively short time and with aminimum number of animals. We have shown that our model is suitable to investigatethe actions of different substances on angiogenesis of the heart, i.e., both substancesthat induce angiogenesis and those that may inhibit it.Subsequently we used our newly developed assay to investigate the role of iNOS onangiogenesis of the mouse heart and aortae under hypoxia. We found that the heart ismore sensitive to the different inhibitors than aortae. In vitro angiogenesis of the heartin iNOS knock out mice, in hypoxia, was totally absent. We therefore concluded thatorgan specific pathways must exist for angiogenesis; and that for angiogenesis of themouse heart, in hypoxia, iNOS is essential.In the last part of the thesis we describe the work done to understand the role ofAngiotensin II in the hypoxic mouse heart. By using different pharmacologicalagonists and antagonists as well as knock out animals we were able to conclude thatthe AT2 receptor is the one responsible for angiogenesis in response to Angiotensin IIin the healthy and hypoxic mouse heart in our in vitro model. Further experiments ledus to conclude that the angiogenic effect of Angiotensin II via the AT2 receptor in thehypoxic mouse heart is mediated via a mechanism that involves the Bradykininreceptor 2.In conclusion we have developed a new in vitro model of angiogenesis in vitro of theheart. Using this model we have analyzed angiogenesis of the hypoxic mouse heartand then characterized effects of Ang II and NO on angiogenesis in vitro." @default.
• W1584614998 created "2016-06-24" @default.
• W1584614998 creator A5053361502 @default.
• W1584614998 date "2005-01-01" @default.
• W1584614998 modified "2023-09-23" @default.
• W1584614998 title "Angiogenesis in vitro of the healthy mouse heart under hypoxia : the role of Angiotensin II and Nitric Oxide" @default.
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